Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (20)
  • Open Access


    Changes in intracellular and extracellular proteins after ERGIC3 knockdown in lung cancer: Proteins interacting with ERGIC3, HORN, and FLNA


    BIOCELL, Vol.47, No.8, pp. 1821-1833, 2023, DOI:10.32604/biocell.2023.027175

    Abstract Objective: Endoplasmic reticulum-Golgi intermediate compartment 3 (ERGIC3) promotes cell proliferation and metastasis in lung cancer, but its molecular mechanism is unclear. Methods: The GLC-82 cells were randomly divided into the ERGIC3i group and the negative control group. The cells were transfected with ERGIC3 siRNA or control siRNA in the groups, respectively. The ERGIC3-interacting proteins expressed in cells or extracellularly were isolated by the immunoprecipitation method and detected by isobaric tags for relative and absolute quantitation and liquid chromatography-tandem mass spectrometry. The differentially expressed proteins were determined by bioinformatic methods. Results: After ERGIC3 knockdown, 88 extracellular differentially expressed proteins, 41 up-regulated… More >

  • Open Access


    RASAL2 acts as a tumor suppressor in cervical cancer cells


    BIOCELL, Vol.47, No.7, pp. 1549-1560, 2023, DOI:10.32604/biocell.2023.027308

    Abstract Background: This study was designed to investigate the roles of RASAL2 in cervical cancer (CC). Methods: Fifty-four CC tissues and 33 adjacent tissues were obtained from CC patients admitted to our hospital between March 2012 and June 2014. Real-time polymerase chain reaction and western blotting were performed to analyze the expression of RASAL2 mRNA and protein in these tissues, CC cell lines, and normal cervical cells. Over-expression and silencing of RASAL2 were induced after transfection, and the migration, invasion, and proliferation of the CC cell lines were examined. Results: RASAL2 mRNA and protein expressions were significantly down-regulated in CC tissues… More >

  • Open Access


    Test Research on the Knock of a Common-Rail Diesel Engine Fueled with Diesel-Methanol Dual-Fuel

    Chao Zhu1, Zhuopei Liu2, Hao Chen2,3, Yangyang Li2,3,*

    Energy Engineering, Vol.120, No.5, pp. 1081-1105, 2023, DOI:10.32604/ee.2023.026000

    Abstract Experiments were conducted on a diesel-methanol dual-fuel (DMDF) engine modified by a six-cylinder, turbo-charged, inter-cooled diesel engine. According to the number of diesel injection, the experiments are divided to two parts: the single injection mode and double injection mode. The results show that, at the double injection mode, the maximum of pressure rise rate is small and the engine runs smoothly, however, knock still occurs when the co-combustion ratio (CCR) is big enough. Under knock status, the power density of the block vibration concentrating at some special frequencies rises dramatically, and the special frequency of single injection mode (about 4.1… More >

  • Open Access


    LncRNA WEE2-AS1 knockdown inhibits the proliferation, migration and invasion of glioma cells via regulating miR-29b-2- 5p/TPM3 axis


    Oncology Research, Vol.29, No.2, pp. 105-117, 2021, DOI:10.32604/or.2022.03536

    Abstract Glioma is a general malignant tumor with a dismal prognosis. Long noncoding RNAs (lncRNAs) have been implicated in the initiation and processes of tumors. An investigation of the GEPIA database revealed that long noncoding RNA WEE2 antisense RNA 1 (WEE2-AS1) is upregulated in glioma tissues compared to normal brain tissues, and validation with quantitative real-time polymerase chain reaction (qRT–PCR) revealed that WEE2-AS1 expression was consistent with the database prediction. Fluorescence in situ hybridization (FISH) assays revealed that WEE2-AS1 was localized primarily in the cytoplasm. Clone formation experiment and EDU assay were used to detect cell proliferation ability, and Transwell assay… More >

  • Open Access


    Knockdown of Long Noncoding RNA CAT104 Inhibits the Proliferation, Migration, and Invasion of Human Osteosarcoma Cells by Regulating MicroRNA-381

    Bo Xia*, Lei Wang, Li Feng*, Baofang Tian*, Yuanjie Tan, Baoyin Du*

    Oncology Research, Vol.27, No.1, pp. 89-98, 2019, DOI:10.3727/096504018X15199511344806

    Abstract Osteosarcoma is the most common primary malignant bone tumor in children and adolescents. This study aimed to explore the effects of long noncoding RNA CAT104 and microRNA-381 (miR-381) on osteosarcoma cell proliferation, migration, invasion, and apoptosis, as well as the underlying potential mechanism. We found that CAT104 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of CAT104 significantly inhibited OS-732 cell proliferation, migration, and invasion, but promoted cell apoptosis. CAT104 regulated the expression of miR-381, and miR-381 participated in the effects of CAT104 on OS-732 cells. Zinc finger E-box-binding homeobox 1 (ZEB1) was a direct target gene of… More >

  • Open Access


    Knockdown of Urothelial Carcinoma-Associated 1 Suppressed Cell Growth and Migration Through Regulating miR-301a and CXCR4 in Osteosarcoma MHCC97 Cells

    Genglong Zhu*, Xialei Liu*, Yonghui Su, Fangen Kong, Xiaopeng Hong*, Zhidong Lin

    Oncology Research, Vol.27, No.1, pp. 55-64, 2019, DOI:10.3727/096504018X15201143705855

    Abstract Liver cancer is one of the most common malignancies in the world and a leading cause of cancer-related mortality. Accumulating evidence has highlighted the critical role of long noncoding RNAs (lncRNAs) in various cancers. The present study aimed to explore the role of lncRNA urothelial carcinoma-associated 1 (UCA1) in cell growth and migration in MHCC97 cells and its underlying mechanism. First, we assessed the expression of UCA1 in MHCC97 and three other cell lines by RT-qPCR. Then the expression of UCA1, miR-301a, and CXCR4 in MHCC97 cells was altered by transient transfection. The effects of UCA1 and miR-301 on cell… More >

  • Open Access


    Knockdown of Long Noncoding RNA ENST457720 Inhibits Proliferation of Non-Small Cell Lung Cancer Cells In Vitro and In Vivo

    Jia Yu, Qiyu Fang, Shuyan Meng

    Oncology Research, Vol.27, No.1, pp. 47-53, 2019, DOI:10.3727/096504018X15193843443255

    Abstract Non-small cell lung cancer (NSCLC) represents the leading cause of cancer-related mortality worldwide. More and more reports have identified important roles for long noncoding RNAs (lncRNAs) in cancer development. ENST457720 expression was upregulated in lung adenocarcinoma in a microarray-based lncRNA screen. We determined the expression levels of ENST457720 in NSCLC tissues with quantitative real-time PCR and then studied their clinical significance. We explored the biological significance of ENST457720 with gain- and lossof-function analyses in vitro and in vivo. In this study, ENST457720 was expressed at higher levels in NSCLC tissues than in paired normal tissues. Higher ENST457720 expression was associated… More >

  • Open Access


    CRISPR/Cas9-Mediated Gene Knockout of ARID1A Promotes Primary Progesterone Resistance by Downregulating Progesterone Receptor B in Endometrial Cancer Cells

    Haizhen Wang*, Zhenghua Tang*, Ting Li*, Menglu Liu*, Yong Li, Baoling Xing*

    Oncology Research, Vol.27, No.9, pp. 1051-1060, 2019, DOI:10.3727/096504019X15561873320465

    Abstract Medroxyprogesterone (MPA) is used for the conservative treatment of endometrial cancer. Unfortunately, progesterone resistance seriously affects its therapeutic effect. The purpose of the current study was to investigate the influence of deletion of AT-rich interactive domain 1A (ARID1A) in progesterone resistance in Ishikawa cells. Ablation of ARID1A was conducted through the CRISPR/Cas9 technology. Acquired progesterone-resistant Ishikawa (Ishikawa-PR) cells were generated by chronic exposure of Ishikawa cells to MPA. The sensitivity of the parental Ishikawa, Ishikawa-PR, and ARID1A-deficient cells to MPA and/or LY294002 was determined using the Cell Counting Kit-8 (CCK-8) assay and flow cytometry analysis. In addition, Western blot analysis… More >

  • Open Access


    Inhibition of Proliferation by Knockdown of Transmembrane (TMEM) 168 in Glioblastoma Cells via Suppression of Wnt/β-Catenin Pathway

    Jie Xu*1, Zhongzhou Su*1, Qiuping Ding, Liang Shen*, Xiaohu Nie*, Xuyan Pan*, Ai Yan*, Renfu Yan*, Yue Zhou*, Liqin Li, Bin Lu*

    Oncology Research, Vol.27, No.7, pp. 819-826, 2019, DOI:10.3727/096504018X15478559215014

    Abstract Human glioblastoma multiforme (GBM) accounts for the majority of human brain gliomas. Several TMEM proteins, such as TMEM 45A, TMEM 97, and TMEM 140, are implicated in human brain gliomas. However, the roles of TMEM168 in human GBM remain poorly understood. Herein we found that mRNA levels of TMEM168 were overexpressed in GBM patients (n=85) when compared with healthy people (n=10), which was also supported by data from The Cancer Genome Atlas (TCGA). Kaplan–Meier analysis of Gene Expression Omnibus dataset GSE16011 suggested that enhanced TMEM168 expression was associated with shorter survival time. To investigate whether and how TMEM168 functioned in… More >

  • Open Access


    Knockdown of lncRNA PVT1 Inhibits Glioma Progression by Regulating miR-424 Expression

    Yanjie Han*1, Xinxin Li*1, Fei He†1, Jiliang Yan*, Chunyan Ma*, Xiaoli Zheng, Jinli Zhang*, Donghui Zhang*, Cuiping Meng*, Zhen Zhang*, Xinying Ji§

    Oncology Research, Vol.27, No.6, pp. 681-690, 2019, DOI:10.3727/096504018X15424939990246

    Abstract Plasmacytoma variability translocation 1 (PVT1), an oncogene, has been reported to be highly expressed in many tumors, including human glioma, gastric cancer, and non-small cell lung cancer. Functionally, it could also regulate the development of tumor cells. However, its specific roles and pathogenesis in human gliomas are still not clear. This study investigated the function and mechanism of PVT1 knockdown in the proliferation and malignant transformation of human gliomas. We first examined the expression levels of PVT1 and miR- 424 in human glioma tissues and cell lines. We also used gene manipulation techniques to explore the effects of PVT1 knockdown… More >

Displaying 1-10 on page 1 of 20. Per Page